Jun-B differs in its biological properties from, and is a negative regulator of, c-Jun

Abstract

c-Jun, Jun-B, and Jun-D proteins bind to the TPA response element (TRE) either as homodimers or as Jun-Fos heterodimers. We demonstrate that c-Jun and Jun-B nevertheless differ markedly in their ability to activate AP-1 responsive genes. c-Jun is an efficient activator of the c-jun and collagenase promoters, which contain a single TRE; Jun-B is not. Furthermore, Jun-B inhibits activation of these promoters by c-Jun. On the other hand, like c-Jun, Jun-B is an efficient activator of constructs containing multimeric TREs. Using chimeric proteins, we show that the distinct behavior of c-Jun and Jun-B is due to differences in their activation domains. Trans-activation by Jun-B depends on cooperative interactions between adjacently bound factors, while activation by c-Jun does not require such interactions. This differential behavior greatly expands the regulatory potential of the Jun family.

Involvement of protein phosphatase 2A nuclear accumulation and subsequent inactivation of activator protein-1 in leptomycin B-inhibited cyclin D1 expression

“…However, selective inhibition of ERK activity with U0126 did not restore the cyclin D1 expression inhibited by LMB, therefore it is not likely that LMB-induced inhibition of cyclin D1 expression is due to LMB-induced activation of ERK 1/2. AP-1 activity can be regulated by the amount of AP-1 protein components in the cells (Chiu et al, 1989;Angel and Karin, 1991). AP-1 consists of dimers between members of the Fos (c-Fos, FosB, Fra-1 and Fra-2), Jun (c-Jun, JunB and JunD) or activating transcription factor families.…”

The effects of glucocorticoid hormone on the expression of c‐jun

“…At least two other members, jun-B and jun-D, have been identified in the jun family. Jun-B was shown to inhibit the trans.activating activities of c-jun when both were eo-transfected into F9 cells [11][12][13][14].…”

Down‐regulation of the protein kinase A pathway by activators of protein kinase C and intracellular Ca2+ in fibroblast cells

“…The expression of c-fos, cjun, andjunB was driven from the RSV (Rous sarcoma virus) enhancer of their vectors RSV-c-fos [8], RSV-c-jun [9], and RSV-junB [10]. Expression of the beta-galactosidase reference gene was driven from the CMV (cytomegalovirus) enhancer of the expression vector pCMVbeta-gal.…”